Keywords

Objectives

To investigate the role of myocardial depressant pro-inflammatory cytokines on myocardial cell damage related to arterial switch operation (ASO) in neonates.

Methods

35 neonates (mean age 7 days) with transposition of the great arteries undergoing ASO were prospectively studied. ASO was performed using combined low-flow cardiopulmonary bypass (CPB) and cardiocirculatory arrest (CCA) under deep hypothermia. Patients with myocardial hypocontractility at the end of the procedure or 4 and 24 h postoperatively (po), as observed at echocardiography, were defined as having myocardial dysfunction (MD). Troponin-T (Tropo-T) and the creatine kinase isoform CKMB served as markers for myocardial cell damage during and after ASO. Interleukine (IL)-6 (a myocardial depressant cytokine) and IL-8 (involved in ischemia-reperfusion damages) served as marker for the systemic inflammatory reaction related to ASO.

Results

Five patients showed MD after ASO, all patients survived. Age at ASO, duration of CPB, CCA or aortic clamping were not different in patients with and without MD. In all patients, plasma levels of Tropo-T increased significantly during CPB (P < 0.0001). At the end of ASO, patients with MD had significantly higher values of Tropo-T than patients without MD (P < 0.002). In contrast to Tropo-T, levels of CKMB did not increase during CPB and were not different in patients with and without MD. IL6 and IL8 increased significantly in all patients during CPB (P < 0.001, respectively). Patients with MD had significantly higher IL6 and IL8 values 4 h po than patients without MD (P < 0.001, respectively). Tropo-T- and IL6 values measured 4 h after ASO were significantly correlated to each other (P < 0.05).

Conclusions

Our results demonstrate myocardial cell damage (as shown by Tropo-T liberation) and systemic inflammatory reaction (as shown by IL6- and IL8-production) related to ASO performed with combined low-flow CPB and CCA under deep hypothermia in neonates. Patients with MD have more important myocardial cell damage and higher magnitude of systemic inflammatory reaction than have patients without this complication. IL6 and IL8 both are possibly directly involved in the damage to the myocardial cell in this setting.